Background Work-related musculoskeletal disorders (WMSDs) are a major occupational health concern, particularly among workers exposed to adverse ergonomic conditions. Manganese production involves heavy physical demands, yet research on WMSDs among manganese workers remains limited. Objective To investigate the prevalence and influencing factors of WMSDs among manganese workers in a manganese enterprise in Guangxi. Methods A cross-sectional survey was conducted from May to June 2024 on workers at a manganese factory in Guangxi. The Chinese Musculoskeletal Disorders Questionnaire was used to collect information on demographic characteristics, distribution of musculoskeletal symptoms, and work-related exposures. χ² test was applied to compare differences in positive WMSDs rates across groups, and logistic regression analysis was performed to identify associated factors. Results A total of 1476 workers were enrolled in the study after pre-determined inclusion and exclusion criteria. The overall prevalence of WMSDs was 34.15%. The most commonly affected body regions were the lower back (17.28%), neck (16.67%), and shoulders (13.82%). The results of logistic regression analysis indicated that female, older age, and education level of college or above were associated with a higher risk of WMSDs (P<0.05). Awkward working postures were significantly associated with WMSDs in corresponding body regions; in particular, awkward postures of the neck, upper limbs, trunk, and lower limbs were related to an increased risk of WMSDs in multiple body sites (P<0.05). In addition, poor lighting conditions, high workplace temperature, frequent or sustained arm support during work, and high job demands were associated with an increased risk of overall or site-specific WMSDs (P<0.05). Conclusion The high prevalence of WMSDs among manganese workers is closely associated with demographic characteristics, working postures, and work environment and organizational factors. Targeted ergonomic interventions focusing on high-risk body regions and key ergonomic exposures are warranted to reduce the risk of WMSDs among manganese workers.

Objective To investigate the role of activating transcription factor 4 (ATF4) in benign prostatic hyperplasia (BPH) in order to elucidate the molecular mechanism underlying BPH progression. Methods Firstly, we analyzed the correlation between the expression of ATF4 and the volume of prostate transition zone in BPH tissues using publicly available datasets. Subsequently, we explored the potential association among ATF4, epithelial-mesenchymal transition (EMT) and BPH through single-cell RNA sequencing (scRNA-seq). Finally, we validated the findings by silencing ATF4 and treating BPH cells with ATF4 protein inhibitors, followed by reverse transcription quantitative polymerase chain reaction (RT-qPCR), CCK-8 assay, and Western blot. Results The expression of ATF4 in BPH tissues exhibited a significant positive correlation with the volume of prostate transition zone (r=0.64, P＜0.05). scRNA-seq analysis revealed that ATF4 was significantly upregulated in the prostate epithelial cells of BPH patients (P＜0.05), and its expression demonstrated a significant positive correlation with the Hallmark EMT singscore (r=0.14, P＜0.05). In vitro experiments further indicated that knockdown of ATF4 led to a significant reduction in the proliferative activity of BPH-1 cells (P＜0.05). Similarly, inhibition of ATF4 activity resulted in a marked decrease in the proliferative capacity and EMT of BPH-1 cells (P＜0.05). Conclusion ATF4 may exert a promoting effect on BPH by modulating the EMT signaling pathway;therefore, ATF4 may serve as a novel therapeutic target of BPH.

Objective: To explore the longitudinal associations between dietary macronutrients and lung function in schoolaged children, so as to provide the nutritional research evidence for promoting children s lung health. Methods: In November 2021, two primary schools located in Chengdu, Sichuan Province were selected from the Southwest China Childhood Nutrition and Growth (SCCNG) cohort by a stratified cluster random sampling method, enrolling a total of 1 112 school aged children aged 8 to 13 years. At baseline, the dietary and sociodemographic characteristics of the children were assessed. One year later, the forced vital capacity (FVC) of the children was measured and converted into Z scores (FVC- Z ), while the vital capacity index (VCI) was also calculated. Generalized linear regression analysis was employed to examine the associations between dietary macronutrients and lung function, considering interactions with gender and age, followed by stratified analysis. Results: After adjusting for confounding factors, the analysis results of the generalized linear regression model showed that the carbohydrate energy ratio was negatively correlated with FVC- Z ( β =-0.02) and VCI ( β =-0.16), while the fat energy ratio showed a positive correlation with FVC- Z ( β =0.03) and VCI ( β =0.23) ( P <0.05). The protein energy ratio was positively correlated with FVC- Z ( β =0.09) and VCI ( β =0.60) specifically in girls ( P <0.05). Additionally, there was an interaction effect of age on the associations between macronutrients and lung function ( P <0.01); in children aged 8-9 and 10-11, the carbohydrate energy supply ratio was negatively correlated with FVC- Z ( β =-0.04, -0.03) and VCI ( β =-0.29, -0.21), and fat energy supply ratio was positively correlated with FVC- Z ( β =0.07, 0.05) and VCI ( β =0.46, 0.32) ( P <0.05). Conclusions There are age and sex differences in the association of dietary macronutrients with lung function, with a low carbohydrate, high fat diet promoting lung function in children. Additionally, protein intake appears to have a positive influence on the lung function of girls. The early school age period may represent a critical window for dietary interventions aimed at promoting lung health.

Objective:To explore the clinical features, histopathological morphology, and differential diagnosis of lymphoepithelioma-like carcinoma with abnormal expression of follicular dendritic cell markers.Methods:From 2020 to 2021, 4 cases of lymphoepithelioma-like carcinoma with abnormal expression of follicular dendritic cell markers diagnosed in Fujian Cancer Hospital (2 cases) and the Second Affiliated Hospital of Fujian Medical University (2 cases) were collected. Different ancillary procedures such as HE, special stains, immunohistochemistry, and in situ hybridization techniques were used to assess the histopathological features and immunophenotypes. The clinical data were collected and literature was reviewed.Results:All 4 cases of lymphoepithelioma-like carcinoma with abnormal expression of follicular dendritic cell markers were male. They were 32, 45, 67 and 39 years old, respectively. The main clinical manifestations were bloody phlegm, abdominal pain, fatigue and anorexia. The clinical stages at diagnosis were stage Ⅳ (3 cases) and stage Ⅱ (1 case). Cases 2 and 3 had two pathological examinations at different sites, with a total of six pathological examinations. The histomorphology showed singly scattered or nests of tumor cells in a background of abundant small lymphocytes. The tumor cells were enlarged and pleomorphic, some appeared polygonal with inconspicuous cell borders, and they were arranged in a syncytial pattern. There were megakaryocytes, multinucleated tumor cells, and a few spindle-shaped cells seen. Atypical mitosis was commonly noted. By immunohistochemistry, the tumor cells were positive for CKpan(5/6), CK8/18(4/4), CAM5.2(2/5), CK-H(0/4), CK-L(3/4), EMA(4/5), CK5/6(3/6), p63(1/6), p40(1/6), E-cadherin (4/6), SSTR2(6/6), PD-L1(5/5), LCA(0/6), vimentin(5/6), CD2 (6/6), CD23(6/6), CD35(5/6), CXCL-13(4/5) and D2-40(1/5). The Ki-67 proliferative index was 60%-95%. In situ hybridization for EBER were all positive (6/6). Special stain for reticulin showed positive staining surrounding nests of tumor cells.Conclusions:The expression of follicular dendritic cell markers in lymphoepithelioma-like carcinoma is very rare, which may be related to EBV infection. Occasionally, it can overlap with follicular dendritic cell sarcoma by morphology and immunophenotype, which can lead to misdiagnosis. Only by combining clinical information, morphological characteristics and immunophenotype can an appropriate diagnosis be made.

After being treated with acupuncture, some patients with idiopathic tinnitus may experience a short-term aggravation of tinnitus symptoms on the original basis. These symptoms can be gradually relieved and the overall condition fluctuates towards recovery. This phenomenon has brought some difficulties to patients and clinicians. Based on the academic view of TCM, "destroying pathogens and re-building balance", and in association with the existing understanding of acupuncture in modern medicine for tinnitus, this paper briefly discusses the mechanism and influencing factors of symptom fluctuation in patients with idiopathic tinnitus after acupuncture treatment in terms of both TCM and modern medicine, and proposes the future direction in the research of symptom fluctuation, so as to promote the recognition of clinicians and patients on symptom fluctuation and make rational use of its positive effects. Besides, it is hoped that more researchers will pay attention to symptom fluctuation and advance the exploration of it in academic field.
Humans ; Tinnitus/physiopathology* ; Acupuncture Therapy ; Male ; Female

Innate lymphoid cells are an important part of innate mucosal immunity and participate in immune response by secreting effector cytokines and regulating the functions of other immune cells.They are similar to T helper cells in transcription factors and secretory cytokines,but they also have some unique functions.Different innate lymphocyte subsets play different roles in chronic obstructive pulmonary disease(COPD)according to their respective characteristics.Compared with adaptive lymphocyte,innate lymphocyte is relatively less in lymphoid tissue,accounting for only a small part of lung immune cells,but these lymphocyte cells play a crucial role in the development and progression of COPD.In this paper,the role of innate lymphoid cells in COPD and the related research progress were reviewed.

Gene therapy, harnessing the power of CRISPR-Cas9 and/or DNAzyme systems, stands as a pivotal approach in cancer therapy, enabling the meticulous manipulation of genes pivotal to tumorigenesis and immunity. However, the pursuit of precise gene therapy encounters formidable hurdles. Herein, a near-infrared upconversion theranostic nanomachine is devised and tailors for CRISPR-Cas9/DNAzyme systems mediate precise gene therapy. An ingenious logic DNAzyme system consists of Chain 1 (C1)/Chain 2 (C2) and endogenous lncRNA is designed. We employ manganese modified upconversion nanoparticles for carrying ultraviolet-responsive C1-PC linker-C2 (C₂P) chain and Cas9 ribonucleoprotein (RNP), with outermost coats with hyaluronic acid. Upon reaching tumor microenvironment (TME), the released Mn²⁺ ions orchestrate a trifecta: facilitating endosomal escape, activating cGAS-STING signaling, and enabling T1-magnetic resonance imaging. Under near-infrared irradiation, Cas9 RNP/C₂P complex dissociates, releasing Cas9 RNP into the nucleus to perform gene editing of Ptpn2, while C1/C2 chains self-assemble with endogenous lncRNA to form a functional DNAzyme system, targeting PD-L1 mRNA for gene silencing. This strategy remodels the TME by activating cGAS-STING signaling and dual immune checkpoints blockade, thus realizing tumor elimination. Our theranostic nanomachine armed with the CRISPR-Cas9/DNAzyme logic systems, represents a resourceful and promising strategy for advancing cancer systemic immunotherapy and precise gene therapy.

Objective:To systematically evaluate the qualitative study of perinatal bereavement care by obstetric nurses and midwives, and explore the barriers to perinatal bereavement care, so as to promote the development of domestic perinatal bereavement care services.Methods:Systematic search of qualitative studies on the experience of obstetric nurses and midwives in caring for perinatal bereaved mothers in PubMed, Web of Science, Embase, Cochrane Library, PsycINFO, CINAHL, China Biomedical Literature Service System, CNKI, Wanfang Database, and VIP database were searched from the establishment until June 30, 2024. The qualitative research quality evaluation was conducted using the 2016 version of the qualitative research quality assessment tool of the Joanna Briggs Institute Evidence-Based Health Care Centre in Australia, and the results of the study were summarized and integrated using the pooled integration method.Results:A total of 14 studies were included, with 3 Chinese literatures and 11 English literatures. A total of 55 themes were extracted, which were summarized and combined into 8 new categories, and 3 integrated results were summarized: insufficient bereavement care ability, insufficient bereavement care confidence, and imperfect allocation of bereavement care resources.Conclusions:The knowledge popularization and training of bereavement care should be strengthened, the organizational support should be strengthened, the confidence of obstetric nurses and midwives in bereavement care should be enhanced, a special perinatal bereavement care team should be set up, and multidisciplinary resources should be integrated to ensure the continuity and coordination of perinatal bereavement care.

BACKGROUND:Delayed healing and nonunion of fractures are common clinical issues.Clinical observations have shown that patients with limb fractures combined with traumatic brain injury experience significantly faster fracture healing compared with those without brain injury.The potential mechanisms behind this phenomenon have become a crucial focus of current research.Recent studies indicate that traumatic brain injury significantly accelerates callus formation and fracture healing processes by regulating cytokines,hormones,neural signals,and stem cell mechanisms.OBJECTIVE:To summarize the latest research progress in the mechanisms by which traumatic brain injury promotes callus formation and fracture healing,thereby providing a theoretical basis for clinical applications.METHODS:The first author conducted a search of CNKI,WanFang,VIP,PubMed,Embase,Web of Science,and Cochrane Library databases for literature published from January 2013 to October 2024,with some references traced back up to 20 years.The search terms used were"traumatic brain injury,callus,fracture healing,inflammatory response,cytokines,hormones,neuropeptides,genes,stem cells"in Chinese and English.A total of 83 articles meeting the inclusion criteria were ultimately selected.RESULTS AND CONCLUSION:The mechanism by which traumatic brain injury promotes callus formation and fracture healing is highly complex,involving multiple regulatory pathways such as cytokines,hormones,the nervous system,and stem cells.However,the precise mechanisms are still not fully understood and require further investigation.Current research suggests that traumatic brain injury accelerates bone callus formation and bone tissue regeneration by promoting the release of cytokines(e.g.,insulin-like growth factor-1)and hormones(e.g.,growth hormone and leptin),regulating the nervous system,and promoting stem cell proliferation and differentiation.Additionally,traumatic brain injury triggers a series of immune responses,including the release of inflammatory factors and activation of immune cells,which modulate fracture healing.These responses improve local blood flow,cell migration,and fibroblast activation,supporting various stages of bone healing.Stem cell activation induced by traumatic brain injury is also crucial,as activated stem cells differentiate into osteoblasts,chondrocytes,and adipocytes,facilitating bone tissue regeneration and repair.Therefore,traumatic brain injury-induced immune responses and stem cell activation work together to accelerate fracture healing,providing essential support for the process.These mechanisms significantly shorten the healing time and improve patient outcomes.In conclusion,traumatic brain injury promotes callus formation and fracture healing through multiple mechanisms,highlighting its importance in bone repair.Future research should focus on the signaling pathways and regulatory factors influenced by traumatic brain injury to further understand its mechanisms.These findings will provide a foundation for developing targeted therapies,stem cell treatments,and neural regulation therapies,with potential clinical value in shortening healing time,optimizing recovery protocols,and improving prognosis.Exploring traumatic brain injury-induced biological effects will open new avenues for fracture treatment.

BACKGROUND:Delayed healing and nonunion of fractures are common clinical issues.Clinical observations have shown that patients with limb fractures combined with traumatic brain injury experience significantly faster fracture healing compared with those without brain injury.The potential mechanisms behind this phenomenon have become a crucial focus of current research.Recent studies indicate that traumatic brain injury significantly accelerates callus formation and fracture healing processes by regulating cytokines,hormones,neural signals,and stem cell mechanisms.OBJECTIVE:To summarize the latest research progress in the mechanisms by which traumatic brain injury promotes callus formation and fracture healing,thereby providing a theoretical basis for clinical applications.METHODS:The first author conducted a search of CNKI,WanFang,VIP,PubMed,Embase,Web of Science,and Cochrane Library databases for literature published from January 2013 to October 2024,with some references traced back up to 20 years.The search terms used were"traumatic brain injury,callus,fracture healing,inflammatory response,cytokines,hormones,neuropeptides,genes,stem cells"in Chinese and English.A total of 83 articles meeting the inclusion criteria were ultimately selected.RESULTS AND CONCLUSION:The mechanism by which traumatic brain injury promotes callus formation and fracture healing is highly complex,involving multiple regulatory pathways such as cytokines,hormones,the nervous system,and stem cells.However,the precise mechanisms are still not fully understood and require further investigation.Current research suggests that traumatic brain injury accelerates bone callus formation and bone tissue regeneration by promoting the release of cytokines(e.g.,insulin-like growth factor-1)and hormones(e.g.,growth hormone and leptin),regulating the nervous system,and promoting stem cell proliferation and differentiation.Additionally,traumatic brain injury triggers a series of immune responses,including the release of inflammatory factors and activation of immune cells,which modulate fracture healing.These responses improve local blood flow,cell migration,and fibroblast activation,supporting various stages of bone healing.Stem cell activation induced by traumatic brain injury is also crucial,as activated stem cells differentiate into osteoblasts,chondrocytes,and adipocytes,facilitating bone tissue regeneration and repair.Therefore,traumatic brain injury-induced immune responses and stem cell activation work together to accelerate fracture healing,providing essential support for the process.These mechanisms significantly shorten the healing time and improve patient outcomes.In conclusion,traumatic brain injury promotes callus formation and fracture healing through multiple mechanisms,highlighting its importance in bone repair.Future research should focus on the signaling pathways and regulatory factors influenced by traumatic brain injury to further understand its mechanisms.These findings will provide a foundation for developing targeted therapies,stem cell treatments,and neural regulation therapies,with potential clinical value in shortening healing time,optimizing recovery protocols,and improving prognosis.Exploring traumatic brain injury-induced biological effects will open new avenues for fracture treatment.